Third, it is possible that the HCMV presence and its interplay with the host cell genome and DNA damage checkpoint and/or repair pathways cause enhanced chromosomal instability in cancer cells such as medulloblastomas in our experiments, and therefore, it might be beneficial for the chronic viral presence in tumour cells to preserve the function of 53BP1 in promoting repair of DNA double‐strand breaks that do occur with enhanced frequencies in cancer cells (Halazonetis et al., 2008). This evidence concerns the gene TP53BP1 and cancer.